| pubmed-article:19640259 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19640259 | lifeskim:mentions | umls-concept:C0235989 | lld:lifeskim |
| pubmed-article:19640259 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
| pubmed-article:19640259 | lifeskim:mentions | umls-concept:C0040690 | lld:lifeskim |
| pubmed-article:19640259 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:19640259 | lifeskim:mentions | umls-concept:C1517004 | lld:lifeskim |
| pubmed-article:19640259 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:19640259 | pubmed:dateCreated | 2009-10-2 | lld:pubmed |
| pubmed-article:19640259 | pubmed:abstractText | Aristolochic acid nephropathy (AAN) is regarded as a kind of rapidly progressive renal fibrosis caused by the ingestion of herbal remedies containing aristolochic acids (AA). A mouse model of AAN was used to assess the patterns of renal injury and TGF-beta1/Smads signaling pathway during the evolution of tubulointerstitial damage and to relate them to the development of fibrosis. A total of 28 mice were randomly assigned to four groups. Three groups were given aristolochic acid I (AAI) at different doses consecutively by gavage for 30 days, while the control group received only phosphate-buffered saline (PBS). Immunohistochemistry and semi-quantitative reverse transcriptase (RT-PCR) detection of the increased expression of fibroblast marker vimentin and de novo expression of alpha-smooth muscle actin (alpha-SMA) with the loss of epithelial maker cytokeratin 18 (CK18) can be utilized to assess AAI-induced tubular necrosis and extensive cortical interstitial fibrosis in a dose-dependent manner. Transforming growth factor-beta1 (TGF-beta1) has been widely recognized as a key fibrogenic cytokine. In our study, TGF-beta1 in the group at dose of 12 mg/kg/ day AAI increased 109.9% compared to control. Smad2 mRNA level in the group at dose of 4.2 mg/kg/day AAI increased 106.4%, and declined 12% in the group at dose of 12 mg/kg/day AAI; Smad4 expression was down-regulated in experimental groups, which declined 13% in the group at dose of 4.2 mg/kg/day AAI. Smad7 mRNA level was down-regulated by AAI in dose-dependence. Collectively, the involvement in interstitial fibrosis progression of active TGF-beta is highly suggested, via the Smads intracellular signaling pathway. These results may be attributed to the dosage of drug and the treatment of renal interstitial fibrosis. | lld:pubmed |
| pubmed-article:19640259 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19640259 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19640259 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:19640259 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19640259 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19640259 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19640259 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19640259 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19640259 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19640259 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19640259 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19640259 | pubmed:issn | 1532-4281 | lld:pubmed |
| pubmed-article:19640259 | pubmed:author | pubmed-author:LiJingJ | lld:pubmed |
| pubmed-article:19640259 | pubmed:author | pubmed-author:YingLiL | lld:pubmed |
| pubmed-article:19640259 | pubmed:author | pubmed-author:WangYanyingY | lld:pubmed |
| pubmed-article:19640259 | pubmed:author | pubmed-author:ZhangZhongwen... | lld:pubmed |
| pubmed-article:19640259 | pubmed:author | pubmed-author:WuGuojuanG | lld:pubmed |
| pubmed-article:19640259 | pubmed:author | pubmed-author:WangDianrenD | lld:pubmed |
| pubmed-article:19640259 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19640259 | pubmed:volume | 29 | lld:pubmed |
| pubmed-article:19640259 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19640259 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19640259 | pubmed:pagination | 280-5 | lld:pubmed |
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| pubmed-article:19640259 | pubmed:meshHeading | pubmed-meshheading:19640259... | lld:pubmed |
| pubmed-article:19640259 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19640259 | pubmed:articleTitle | TGF-beta 1/Smads signaling stimulates renal interstitial fibrosis in experimental AAN. | lld:pubmed |
| pubmed-article:19640259 | pubmed:affiliation | Laboratory of Pharmacology of the Chinese Veterinary Medicine, Department of Animal Science and Technology, Beijing University of Agriculture, Beijing 102206, PR China. | lld:pubmed |
| pubmed-article:19640259 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19640259 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:19640259 | lld:pubmed |
